Primary hemostasis: platelets carried in the flow adhere to exposed collagen at the injury and recruit nearby platelets into a growing plug. Secondary hemostasis runs alongside it as two coupled kinetic quantities, thrombin T and fibrin F:
dT/dt = k1·injury·plugMass − k2·(1+heparin)·T — tissue-factor-driven thrombin generation, inhibited by antithrombin (boosted by heparin).dF/dt = k3·T·(1−F) − k4·flow·F·(1−plugMass) − k5·F — thrombin polymerizes fibrinogen into fibrin, which flow can wash away until the plug covers enough of the wound, plus slow natural fibrinolysis.
Heparin does not stop platelets from plugging the wound — it blocks thrombin generation, so at a high dose the plug forms but fibrin never stabilizes it and flow keeps eroding it (a rebleed). Low flow with a large plug and low heparin lets the clot overgrow the injury into the open lumen — a simplified picture of the stasis + hypercoagulability + wall injury combination classically known as Virchow's triad.